The leading cause of death in adults in the U.S.A. is coronary artery disease; yet the disease remains silent or dormant in the majority of patients until the fourth or fifth decade of life. Then, coronary artery disease typically moves from the "silent" phase to a symptomatic phase, at which time the patient may experience as the first symtoms, angina pectoris, myocardial infarction, and/or sudden death.
The prevalence of coronary artery disease in the United States has been estimated at over 4,000,000 persons. Over 1,000,000 are expected to have myocardial infarctions each year and of these, approximately 500,000 persons are expected to survive through the first few hours and the subsequent hospitalization. Put another way, a U.S. male has a 1 in 5 chance of having a myocardial infarction or suffering sudden death before the age of 60. Further, once coronary artery disease is symptomatic--regardless of whether the symptom is angina or myocardial infarction--the mortality rate is increased to 4% per year overall and 8% per year in those with an abnormal electrocardiogram or hypertension. This increased mortality is due to sudden death or the complications of repeated myocardial infarction.
Nearly all symptomatic coronary artery disease is due to coronary atherosclerosis, a pathologic process which results in the narrowing of the coronary arteries (the arteries which supply the heart itself with blood) due to the presence of excess cellular and connective tissue materials and an abnormal accumulation of cholesterol. The presence of these narrowings in addition to spasm of the arteries in the area of the narrowings results in an inadequate blood supply to the myocardium or muscle of the heart. This inadequate blood supply is called ischemia and is expressed by a spectrum of conditions including angina, myocardial infarction and sudden death. However, and most significantly, myocardial ischemia may be entirely "silent", i.e. the patient may be totally unaware of a sudden and potentially dangerous decrease in the blood supply to his heart.
Regardless of the initial expression of the coronary artery disease, patients with symptoms are at an increased risk for myocardial infarction and/or sudden death. The current approach to the therapy of this condition has been to make a definitive diagnosis by historical criteria, stress testing, radionuclide studies, and coronary arteriography and then to treat the patient with medication and/or coronary artery bypass surgery. Despite major advances in surgical technique, and the availability of long acting nitrates, betaadrenergic blockers, and calcium antagonists, the death rate from cardiovascular disease has declined only slightly. This suggests the need for new therpeutic approaches.
Traditionally, physicians have recognized the presence of acute myocardial ischemia by noting the occurrence of angina in the patient. Indeed, success of therapy is often gauged by how well the symptom of angina is controlled, i.e. how effective medication or surgery has been at decreasing the frequency and severity of anginal attacks. This is because when angina occurs, it indicates that ischemia is present, and when ischemia is present the chance of myocardial infarction or sudden death is increased. In theory, decrease in attacks of angina should translate into a decrease in myocardial infarction and sudden death; in point of fact, the decrease has been small.
The development of apparatus to perform analyses on electrocardiographic (EKG) signals has facilitated recognition of myocardial ischemia in a patient. Through these analyses it has become widely accepted that a depression of the portion of the EKG signal known as the ST segment, relative to the isoelectric segment of the signal, correlates with partial lack of blood supply, while elevation of the ST segment relative to the isoelectric segment of the signal correlates with a complete lack of blood supply.
Once the ST segment was identified as an indicator of myocardial ischemia, it was then verified that during anginal attacks the ST segment was altered; a deviation of the ST segment could actually precede the experience of angina by several minutes, or even be entirely silent. Silent episodes are no less dangerous then anginal episodes, and occur in patients with equally as extensive coronary disease as those with anginal episodes, and are frequently accompanied by ventricular rhythm disturbances.
An individual patient may express ischemia silently at all times, may have angina during many ischemic episodes, or have both silent and symptomatic episodes. Recently it has been suggested that these silent episodes may be a predictor of myocardial infarction and death.
The patient's failure to sense the myocardial ischemia by experiencing discomfort has been called the result of a defective anginal warning system as it were, and such a defect may be one of the reasons for the high incidence of myocardial infarction and sudden death.
Concern for patients with coronary artery disease and rhythm disturbances has led to the development of various devices for the monitoring of EKG signals. These devices typically are classified into three groups:
(1) devices which record EKG signals continuously for predetermined periods of time on magnetic tape for subsequent printing and analysis by specially trained technicians and/or computers (see U.S. Pat. No. 3,267,934 to Thornton);
(2) devices which analyze the EKG signal as it is generated by the patient and which store selected data for subsequent analysis (see U.S. Pat. Nos. 4,073,001 and 4,006,737 to Cherry et al); and
(3) patient activated devices which record, store and or transmit EKG signals to a remote location for analysis when the patient notices something abnormal, or on a preselected basis (see U.S. Pat. No. 3,724,454 to Unger).
The first two groups of devices require sophisticated and costly off-line analysis of large amounts of data which may be available only after the event(s) being monitored has occurred. The third group of devices has the limitations that only symptomatic events detected by the patient are available for analysis, or the preselected schedule established for monitoring signals may permit major EKG events to be missed entirely.